From the Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, New Jersey Medical School, Rutgers Biomedical and Health Sciences, Newark.
Circ Res. 2013 Nov 8;113(11):1192-5. doi: 10.1161/CIRCRESAHA.113.302501.
A series of studies conducted 20 years ago, documenting the cardiac hypertrophy phenotype and its underlying signaling mechanism induced by angiotensin II (Ang II) and mechanical stress, showed a remarkable similarity between the effect of the Gαq agonist and that of mechanical forces on cardiac hypertrophy. Subsequent studies confirmed the involvement of autocrine/paracrine mechanisms, including stretch-induced release of Ang II in load-induced cardiac hypertrophy. Recent studies showed that the Ang II type 1 (AT1) receptor is also directly activated by mechanical forces, suggesting that AT1 receptors play an important role in mediating load-induced cardiac hypertrophy through both ligand- and mechanical stress-dependent mechanisms.
二十年前进行的一系列研究记录了血管紧张素 II（Ang II）和机械应激诱导的心脏肥大表型及其潜在的信号机制，结果表明 Gαq 激动剂和机械力对心脏肥大的作用之间存在显著的相似性。随后的研究证实了自分泌/旁分泌机制的参与，包括负荷诱导的心脏肥大中牵张诱导的 Ang II 释放。最近的研究表明，血管紧张素 II 型 1（AT1）受体也可被机械力直接激活，这表明 AT1 受体通过配体和机械应激依赖的机制在介导负荷诱导的心脏肥大中发挥重要作用。
